There is converging evidence that structural alterations of cortical microcircuitry in schizophrenia lead to impaired oscillatory synchronization of neurons in these networks. Such impaired oscillatory synchronization may be an important factor underlying both the psychotic symptoms and the cognitive deficits characteristic of schizophrenia. Oscillatory synchronization, operating across multiple spatial and temporal scales, organizes neuronal activity in local microcircuits, and supports long-range dynamical connections, which are also impaired in schizophrenia. In addition, impaired oscillations may also adversely affect the development of cortical networks and their long-range connections. The recent shift in the conceptualization of schizophrenia from errors in dopamine neurotransmission to core deficits in information processing gave rise to a new generation of animal models focusing on the neurodevelopmental aspects and on the role of other systems, such as NMDA and GABA. Importantly, these models, in addition to schizophrenia-relevant behaviors, exhibit the animal equivalents of schizophrenia-related neurocognitive deficits and show characteristic abnormalities in the organization of the GABAergic interneuron networks of the cortex, reminiscent of those in schizophrenic patients. GABAergic interneurons are involved in the generation of brain oscillations which in turn are known to be critical for cognitive processes. Their alterations in schizophrenic patients were proposed to significantly contribute to the neurocognitive impairments and psychotic symptoms, characteristic for this disease. I will present data of our current projects examining the mechanisms of oscillatory synchronization in different rodent models of schizophrenia produced by acute, sub-acute, chronic, and neurodevelopmental manipulations interfering with early development of the GABAergic network or altering its function by subunit-specific blockade of NMDA receptors.